ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Homology-mediated end-capping as a primary step of sister chromatid fusion in the breakage-fusion-bridge cycles (2013)
    Oxford University Press
    Details
    Publication Date: 2013-11-21
    Description: Breakage-fusion-bridge (BFB) cycle is a series of chromosome breaks and duplications that could lead to the increased copy number of a genomic segment (gene amplification). A critical step of BFB cycles leading to gene amplification is a palindromic fusion of sister chromatids following the rupture of a dicentric chromosome during mitosis. It is currently unknown how sister chromatid fusion is produced from a mitotic break. To delineate the process, we took an integrated genomic, cytogenetic and molecular approach for the recurrent MCL1 amplicon at chromosome 1 in human tumor cells. A newly developed next-generation sequencing-based approach identified a cluster of palindromic fusions within the amplicon at ~50-kb intervals, indicating a series of breaks and fusions by BFB cycles. The physical location of the amplicon (at the end of a broken chromosome) further indicated BFB cycles as underlying processes. Three palindromic fusions were mediated by the homologies between two nearby inverted Alu repeats, whereas the other two fusions exhibited microhomology-mediated events. Such breakpoint sequences indicate that homology-mediated fold-back capping of broken ends followed by DNA replication is an underlying mechanism of sister chromatid fusion. Our results elucidate nucleotide-level events during BFB cycles and end processing for naturally occurring mitotic breaks.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Deconstructing myotonic dystrophy (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: Triplet repeat diseases are disorders in which there is expansion of a repeat sequence of three nucleotides in the affected gene. Although the pathology usually results from production of a defective protein, myotonic dystrophy (DM) has proved to be a puzzle because the expanded repeats appear in a non-coding region of the affected DMPK gene. In a Perspective, Tapscott explains how findings from a new mouse model of DM (Mankodi et al.) could solve this paradox.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1701-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. stapscot@fhcrc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11001736" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Anticipation, Genetic ; Cataract/etiology ; Chromosomes, Human, Pair 19 ; Chromosomes, Human, Pair 3 ; Disease Models, Animal ; Gene Expression Regulation ; Heart Conduction System/physiopathology ; Homeodomain Proteins/genetics ; Humans ; Mice ; Mice, Knockout ; Muscle, Skeletal/metabolism/pathology/physiopathology ; Myotonic Dystrophy/*genetics/metabolism/pathology/physiopathology ; Myotonin-Protein Kinase ; Phenotype ; Protein-Serine-Threonine Kinases/*genetics/metabolism ; RNA Processing, Post-Transcriptional ; RNA, Messenger/*genetics/metabolism ; RNA-Binding Proteins/metabolism ; *Trinucleotide Repeat Expansion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Biomedicine. Reconstructing myotonic dystrophy (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Thornton, C A -- New York, N.Y. -- Science. 2001 Aug 3;293(5531):816-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. stapscot@fhcrc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11486078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Humans ; *Introns ; Mice ; *Microsatellite Repeats ; Mutation ; Myotonic Dystrophy/*genetics/metabolism ; Myotonin-Protein Kinase ; Protein-Serine-Threonine Kinases/genetics ; RNA/*genetics ; RNA-Binding Proteins/chemistry/*genetics/metabolism ; Trinucleotide Repeats ; *Zinc Fingers
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    5-bromo-2'-deoxyuridine blocks myogenesis by extinguishing expression of MyoD1 (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-04
    Description: The pyrimidine analog 5-bromodeoxyuridine (BUdR) competes with thymidine for incorporation into DNA. Substitution of BUdR for thymidine does not significantly affect cell viability but does block cell differentiation in many different lineages. BUdR substitution in a mouse myoblast line blocked myogenic differentiation and extinguished the expression of the myogenic determination gene MyoD1. Forced expression of MyoD1 from a transfected expression vector in a BUdR-substituted myoblast overcame the block to differentiation imposed by BUdR. Activation of BUdR-substituted muscle structural genes and apparently normal differentiation were observed in transfected myoblasts. This shows that BUdR blocks myogenesis at the level of a myogenic regulatory gene, possibly MyoD1, not by directly inhibiting the activation of muscle structural genes. It is consistent with the idea that BUdR selectively blocks a class of regulatory genes, each member of which is important for the development of a different cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Lassar, A B -- Davis, R L -- Weintraub, H -- New York, N.Y. -- Science. 1989 Aug 4;245(4917):532-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2547249" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bromodeoxyuridine/metabolism/*pharmacology ; Cell Differentiation/drug effects ; Cell Line ; Creatine Kinase/genetics ; DNA/metabolism ; Desmin/genetics ; Gene Expression Regulation/*drug effects ; Genes ; Mice ; Muscle Proteins/*genetics ; Muscles/*cytology ; Myogenin ; Nuclear Proteins/*genetics ; Plasmids ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Deficiency in rhabdomyosarcomas of a factor required for MyoD activity and myogenesis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Rhabdomyosarcoma cells express the myogenic helix-loop-helix proteins of the MyoD family but do not differentiate into skeletal muscle cells. Gel shift and transient transfection assays revealed that MyoD in the rhabdomyosarcoma cells was capable of binding DNA but was relatively nonfunctional as a transcriptional activator. Heterokaryon formation with fibroblasts resulted in the restoration of transcriptional activation by MyoD and the differentiation of the rhabdomyosarcoma cells into skeletal muscle cells. These results suggest that rhabdomyosarcomas are deficient in a factor required for MyoD activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Thayer, M J -- Weintraub, H -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1450-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Differentiation ; Cell Nucleus/metabolism/ultrastructure ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Humans ; Mice ; Muscle Proteins/genetics/*metabolism ; Muscles/pathology ; MyoD Protein ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Rhabdomyosarcoma/genetics/*metabolism/pathology ; Transcription Factors/*metabolism ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    MyoD1: a nuclear phosphoprotein requiring a Myc homology region to convert fibroblasts to myoblasts (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-21
    Description: Expression of a complementary DNA (cDNA) encoding the mouse MyoD1 protein in a variety of fibroblast and adipoblast cell lines converts them to myogenic cells. Polyclonal antisera to fusion proteins containing the MyoD1 sequence show that MyoD1 is a phosphoprotein present in the nuclei of proliferating myoblasts and differentiated myotubes but not expressed in 10T1/2 fibroblasts or other nonmuscle cell types. Functional domains of the MyoD1 protein were analyzed by site-directed deletional mutagenesis of the MyoD1 cDNA. Deletion of a highly basic region (residues 102 to 135) interferes with both nuclear localization and induction of myogenesis. Deletion of a short region (residues 143 to 162) that is similar to a conserved region in the c-Myc family of proteins eliminates the ability of the MyoD1 protein to initiate myogenesis but does not alter nuclear localization. Deletions of regions spanning the remainder of MyoD1 did not affect nuclear localization and did not inhibit myogenesis. Furthermore, expression of only 68 amino acids of MyoD1, containing the basic and the Myc similarity domains, is sufficient to activate myogenesis in stably transfected 10T1/2 cells. Genetic analysis maps the MyoD1 gene to mouse chromosome 7 and human chromosome 11.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Davis, R L -- Thayer, M J -- Cheng, P F -- Weintraub, H -- Lassar, A B -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):405-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Chromosome Mapping ; DNA/genetics ; Fibroblasts/cytology ; *Genes ; Humans ; Mice ; Muscles/cytology ; *MyoD Protein ; Nuclear Proteins/*genetics/physiology ; *Oncogenes ; Phosphoproteins/*genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    A unifying genetic model for facioscapulohumeral muscular dystrophy (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-21
    Description: Facioscapulohumeral muscular dystrophy (FSHD) is a common form of muscular dystrophy in adults that is foremost characterized by progressive wasting of muscles in the upper body. FSHD is associated with contraction of D4Z4 macrosatellite repeats on chromosome 4q35, but this contraction is pathogenic only in certain "permissive" chromosomal backgrounds. Here, we show that FSHD patients carry specific single-nucleotide polymorphisms in the chromosomal region distal to the last D4Z4 repeat. This FSHD-predisposing configuration creates a canonical polyadenylation signal for transcripts derived from DUX4, a double homeobox gene of unknown function that straddles the last repeat unit and the adjacent sequence. Transfection studies revealed that DUX4 transcripts are efficiently polyadenylated and are more stable when expressed from permissive chromosomes. These findings suggest that FSHD arises through a toxic gain of function attributable to the stabilized distal DUX4 transcript.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4677822/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4677822/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lemmers, Richard J L F -- van der Vliet, Patrick J -- Klooster, Rinse -- Sacconi, Sabrina -- Camano, Pilar -- Dauwerse, Johannes G -- Snider, Lauren -- Straasheijm, Kirsten R -- van Ommen, Gert Jan -- Padberg, George W -- Miller, Daniel G -- Tapscott, Stephen J -- Tawil, Rabi -- Frants, Rune R -- van der Maarel, Silvere M -- P01 NS069539/NS/NINDS NIH HHS/ -- P01NS069539/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1650-3. doi: 10.1126/science.1189044. Epub 2010 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724583" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Base Sequence ; Child, Preschool ; Chromosomes, Human, Pair 10/genetics ; Chromosomes, Human, Pair 4/*genetics ; Female ; Genetic Predisposition to Disease ; Haplotypes ; Homeodomain Proteins/*genetics/physiology ; Humans ; Male ; Middle Aged ; Models, Genetic ; Molecular Sequence Data ; Muscular Dystrophy, Facioscapulohumeral/*genetics ; Polyadenylation ; Polymorphism, Single Nucleotide ; RNA Stability ; RNA, Messenger/genetics/metabolism ; *Repetitive Sequences, Nucleic Acid ; Transcription, Genetic ; Transfection ; Young Adult
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Different proteins associated with 10-nanometer filaments in cultured chick neurons and nonneuronal cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-01
    Description: A protein of molecular size 180 kilodaltons is associated with 10-nanometer filaments in neurons and is immunologically distinct from smaller putative neurofilament subunits and from 10-nanometer filament proteins in nonneuronal cells, such as myotubes and fibroblasts. Neurons do not contain vimentin, the major filament protein in many other cells, including the nonneuronal cells in cultures of neural tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bennett, G S -- Tapscott, S J -- Kleinbart, F A -- Antin, P B -- Holtzer, H -- HD07152/HD/NICHD NIH HHS/ -- HL15835/HL/NHLBI NIH HHS/ -- HL18708/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1981 May 1;212(4494):567-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6163217" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoskeleton/*ultrastructure ; Desmin ; Epitopes ; Fibroblasts/analysis ; Glial Fibrillary Acidic Protein ; Keratins/analysis ; Molecular Weight ; Muscle Proteins/analysis ; Nerve Tissue Proteins/*analysis/immunology ; Neurofilament Proteins ; Spinal Cord/analysis ; Vimentin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    Electronic Resource
    Electronic Resource
    Neuronal precursor cells in the chick neural tube express neurofilament proteins (1981)
    [s.l.] : Nature Publishing Group
    Nature 292 (1981), S. 836-838 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Our findings are based on immunofluorescent localization of IF proteins using previously characterized antisera against FIF protein the 180,000-molecular weight (MW)10'21 and 70,000-MW21 NIF proteins, and IF proteins characteristic of astrocytes21 and muscle cells23'24. Cryostat sections were taken ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/292836a0
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    facet.materialart.
    Unknown
    Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure. (1995)
    National Academy of Sciences
    Details
    Publication Date: 1995-06-06
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...